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. 2023 Apr 19;40(4):421–433. doi: 10.1007/s10719-023-10113-y

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Role of ST3GalVI in SLeX expression and malignant properties of LS174T cells. (a) Expression analysis of St3GalIII in a panel of GI cancer cell lines showing a heterogeneous expression within cell lines, with LS174T presenting the lowest expression. (b) Expression analysis of St3GalVI in a panel of GI cancer cell lines showing a heterogeneous expression within cell lines, with LS174T presenting a significant expression. Bar graph shows the mean relative quantification values for each gene, normalized to the internal control gene ACTB. (c) immunofluorescence analysis of LS174T ST3GalVI KO cells showing a reduced SLeX expression in ST3GalVI KO clones and a complete abolishment of expression in ST3GalIV/VI KO clones. The scale bar corresponds to 50 μm. (d) Expression levels and percentage of SLeX positive cells measured by flow cytometry analysis, showing a complete abolishment of SLeX detection in the double KO cells. (e) Western blot analysis of ST3GalVI KO clones showing the capacity of ST3GaVI and ST3GalIV/VI KO in impair SLeX expression at the protein level. (f), (h) Proliferation analysis in ST3GalVI KO clones showing no statistically significant differences. (g), (i) Motility capacity of ST3GalVI KO clones showing a reduced cell motility only in ST3GalIV/VI KO clones